The toxicity of oxygen and more specifically its partial reduction products known as reactive oxygen species (ROS) is commonly designated as oxidative stress. It arises from an imbalance of cellular pro-oxidant and antioxidant processes. Oxidative stress has been implicated in a variety of pathological and chronic degenerative processes including the development of cancer, atherosclerosis, inflammation, aging, neurodegenerative disorders, cataracts, retinal degeneration, drug action and toxicity, reperfusion injury after tissue ischemia, and defense against infection. See, for instance, Gao X, Dinkova-Kostova A T, Talalay P. (2001) Proc Natl Acad Sci USA., 98(26):15221-6, which is incorporated herein by reference. The publications listed at page 15226 of Gao et al., 2001, supra, also are incorporated herein by reference. Mammalian cells contribute to their own oxidative stress by generating ROS as part of normal aerobic metabolism, and have developed elaborate and overlapping mechanisms for combating these hazards (Halliwell, B. & Gutteridge, J. M. C. (1999) Free Radicals in Biology and Medicine. Oxford University Press, New York, pp. 1-36). Nevertheless, protective mechanisms are not completely effective especially during increased oxidative stress. The desirability of developing methods for augmenting these defenses is reflected in the widespread human consumption and perceived health benefits of plant-based antioxidants such as ascorbic acid, tocopherols, carotenoids, and polyphenols (Pokorny, J., Yanishlieva, M. & Gordon, M. (2001) Antioxidants in food: practical applications. Woodhead Publishing, Ltd., Cambridge, U.K). These direct antioxidants neutralize free radicals and other chemical oxidants but are consumed in these reactions. Additional compounds are needed to protect subjects from oxidative stress disorders as well as for treatment of subjects suffering from these same disorders.